Skin is the largest organ in the human body and the primary physical barrier against infection and disease. Aging is associated with the deterioration of the dermal and epidermal layers of the skin, resulting from reductions in cell proliferation, collagen synthesis, extracellular matrix remodelling and altered epidermal morphology. Additionally, recent research indicates that aged and senescent dermal fibroblasts exhibit reduced energy metabolism, higher mitochondrial oxidative stress, and mitochondrial DNA (mtDNA) deletions, reflecting characteristics of the mitochondrial free radical theory of aging. In agreement, the deletion of a free radical scavenger within the mitochondria, superoxide dismutase 2, from connective tissue results in premature skin aging and depleting mtDNA in dermal fibroblasts mimics the gene profile of photoaging. Conversely, treatment with PPAR agonists that stimulate mitochondrial metabolism and cell proliferation improves skin wound healing and retards age-related tissue degeneration. Therefore, interventions that improve skin metabolism and mitochondrial function provide a promising means to maintain skin health in old age.
Endurance exercise induces metabolic adaptations via activation of the transcriptional co-activator, peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α). PGC-1α is the master regulator of mitochondrial metabolism and biogenesis, and has been touted as a potential therapeutic target for aging-associated diseases, including diabetes. Interestingly, mild over-expression of PGC-1α in skeletal muscle alone is known to be protective against sarcopenia, to attenuate inactivity-induced fiber atrophy, to ameliorate ALS pathology, to reduce systemic chronic inflammation, and to maintain systemic glucose and insulin homeostasis in aged mice.
Accordingly, it would be desirable to further understand the metabolic effects of exercise in order to develop novel therapies capable of inducing mitochondrial biogenesis and improving skin and muscle health.